Mechanistically, VSV-S remodels the immunosuppressive tumor microenvironment by decreasing myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs), favoring neutrophil and CD8+ T cell infiltration, increasing IFN-γ, lowering TGF-β, and inducing apoptosis and potentiating the efficacy of immune checkpoint blockade [81,82]. This evidence concerns the gene TGFB1 and neoplasm.